- Author:
Huabo CAI
1
;
Baoxing HUANG
;
Zhongsheng ZHU
;
Dongling DAI
;
Shaoming ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Alanine Transaminase; Animals; Aspartate Aminotransferases; Child; Child, Preschool; Creatine Kinase; Heart Failure; Hepatitis; Herpesvirus 4, Human; Humans; Hypoxia; Infant; L-Lactate Dehydrogenase; Respiratory Insufficiency; Retrospective Studies
- From: Chinese Journal of Pediatrics 2016;54(3):201-204
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the etiology and clinical characteristics of hypoxic hepatitis (HH) in children.
METHODClinical data of 7 patients with HH in Shenzhen Children's Hospital from January 2011 to March 2014 were retrospectively reviewed.
RESULTSeven cases diagnosed as HH, age from 4 months to 11 years, were admitted to pediatric intensive care unit (PICU), and accounted for 0.32% of patients in PICU during the same period. The primary causes of HH were respiratory failure and cardiac shock caused by severe hand-foot-and-mouth disease, fulminant myocarditis, infant muggy syndrome . Serologic tests for hepatitis B virus, hepatitis C virus, as well as serum antibody and DNA for Epstein-Barr virus and cytomegalovirus were all negative. There was an increase of alanine aminotransferase (ALT) (≥20 time supper limit of normal (ULN), the highest ALT was more than 130 times ULN in all the patients, which was decreased to 2 times ULN from peak within 10 days. There was a significant relationship between ALT and aspartate aminotransferase(AST)in 3 cases(r=1.000, 1.000, and 0.833, respectively, P<0.05), ALT and lactate dehydrogenase (LDH)in 2 cases(r=1.000 and 0.886, respectively, P<0.05), ALT and blood urea nitrogen(BUN)in 1 case(r=1.000, P<0.05), and ALT and creatine kinase(CK)in 1 case(r=0.964, P<0.05). The ALT, AST and LDH returned to normal soon after the primary diseases were controlled.
CONCLUSIONSevere heart failure, hypoxemia, shock, etc. are the leading primary diseases causing HH. The sharp increase in ALT, AST and LDH is the typical laboratory manifestion in HH after the onset, which may decline to normal shortly after the treatment, sometimes complicated with reversible change in BUN or CK.